Statin intensity and postoperative mortality following open repair of intact abdominal aortic aneurysm.

BackgroundThere is a lack of evidence for the association between intensive statin therapy and outcomes following vascular surgery. The aim of this study was to evaluate the association between perioperative statin intensity and in-hospital mortality following open abdominal aortic aneurysm (AAA) repair.MethodsPatients undergoing open AAA repair between 2009 and 2015 were identified from the Premier Healthcare Database. Statin use was classified into low, moderate and high intensity, based on American College of Cardiology/American Heart Association guidelines. Supratherapeutic intensity was defined as doses higher than the recommended guidelines. Multivariable logistic regression analyses were undertaken to assess the association between statin intensity and postoperative major adverse events and in-hospital mortality.ResultsOf 6497 patients undergoing open AAA repair, 3217 (49·5 per cent) received perioperative statin. Statin users were more likely to present with three or more co-morbidities than non-users (26·5 versus 21·8 per cent; P < 0·001). Unadjusted postoperative mortality was significantly lower in statin users (2·6 versus 6·3 per cent; P < 0·001); however, there was no difference in the risk of developing major adverse events. Multivariable analysis showed that statin use was associated with lower odds of death (odds ratio 0·41, 95 per cent c.i. 0·31 to 0·54). Moderate, high and supratherapeutic statin intensities were not associated with lower odds of death or major adverse events compared with low-intensity statin therapy.ConclusionStatin use is associated with lower odds of death in hospital following open AAA repair. High-intensity statins were not associated with lower morbidity or mortality

How Good Are Provider Annotations?: A Machine Learning Approach

Introduction: CMS-2728 form (Medical Evidence Report) assesses 23 comorbidities chosen to reflect poor outcomes and increased mortality risk. Previous studies questioned the validity of physician reporting on forms CMS-2728. We hypothesize that reporting of comorbidities by computer algorithms identifies more comorbidities than physician completion, and, therefore, is more reflective of underlying disease burden. Methods: We collected data from CMS-2728 forms for all 296 patients who had incident ESRD diagnosis and received chronic dialysis from 2005 through 2014 at Indiana University outpatient dialysis centers. We analyzed patients' data from electronic medical records systems that collated information from multiple health care sources. Previously utilized algorithms or natural language processing was used to extract data on 10 comorbidities for a period of up to 10 years prior to ESRD incidence. These algorithms incorporate billing codes, prescriptions, and other relevant elements. We compared the presence or unchecked status of these comorbidities on the forms to the presence or absence according to the algorithms. Findings: Computer algorithms had higher reporting of comorbidities compared to forms completion by physicians. This remained true when decreasing data span to one year and using only a single health center source. The algorithms determination was well accepted by a physician panel. Importantly, algorithms use significantly increased the expected deaths and lowered the standardized mortality ratios. Discussion: Using computer algorithms showed superior identification of comorbidities for form CMS-2728 and altered standardized mortality ratios. Adapting similar algorithms in available EMR systems may offer more thorough evaluation of comorbidities and improve quality reporting

Unidad Didáctica Adaptada para la Educación Física en un Centro de Educación Especial

In this work we proceed to describe an Adapted Didactic Unit, on the content block "The Body: Image and Perception", belonging to a Physical Education program for the students of a special education centre with affected children, in different degrees, of Intellectual Disability , Generalized Developmental Disorder and Multidisability. The purpose of this article is to present a successful experience to other special education centres with similar characteristics.En este trabajo se procede a describir una Unidad Didáctica Adaptada, sobre el bloque de contenidos “El Cuerpo: Imagen y Percepción“, perteneciente a un programa de Educación Física para los alumnos de un centro de educación especial con niños afectados, en diferentes grados, de Discapacidad Intelectual, Trastorno Generalizado del desarrollo y Plurideficiencia. El propósito de este artículo es dar a conocer una experiencia exitosa a otros centros de educación especial de características similares

Acute limb ischemia from gunshot wound secondary to arterial vasospasm.

Gunshot wounds are rising in incidence, morbidity, and mortality. It is thought that about half of nonfatal injuries occur in an extremity. Although the incidence is not known, arterial vasospasm can result in acute limb ischemia. We present the case of a 33-year-old man who suffered a gunshot wound to the left lower extremity resulting in arterial vasospasm of the superficial femoral artery. He quickly regained arterial flow, and we were able to manage his acute limb ischemia nonoperatively and to document restoration of flow through serial examinations and Doppler imaging. He was subsequently discharged the next day and is experiencing a full recovery

Neuronal migration and ventral subtype identity in the telencephalon depend on SOX1

Little is known about the molecular mechanisms and intrinsic factors that are responsible for the emergence of neuronal subtype identity. Several transcription factors that are expressed mainly in precursors of the ventral telencephalon have been shown to control neuronal specification, but it has been unclear whether subtype identity is also specified in these precursors, or if this happens in postmitotic neurons, and whether it involves the same or different factors. SOX1, an HMG box transcription factor, is expressed widely in neural precursors along with the two other SOXB1 subfamily members, SOX2 and SOX3, and all three have been implicated in neurogenesis. SOX1 is also uniquely expressed at a high level in the majority of telencephalic neurons that constitute the ventral striatum (VS). These neurons are missing in Sox1-null mutant mice. In the present study, we have addressed the requirement for SOX1 at a cellular level, revealing both the nature and timing of the defect. By generating a novel Sox1-null allele expressing β-galactosidase, we found that the VS precursors and their early neuronal differentiation are unaffected in the absence of SOX1, but the prospective neurons fail to migrate to their appropriate position. Furthermore, the migration of non-Sox1-expressing VS neurons (such as those expressing Pax6) was also affected in the absence of SOX1, suggesting that Sox1-expressing neurons play a role in structuring the area of the VS. To test whether SOX1 is required in postmitotic cells for the emergence of VS neuronal identity, we generated mice in which Sox1 expression was directed to all ventral telencephalic precursors, but to only a very few VS neurons. These mice again lacked most of the VS, indicating that SOX1 expression in precursors is not sufficient for VS development. Conversely, the few neurons in which Sox1 expression was maintained were able to migrate to the VS. In conclusion, Sox1 expression in precursors is not sufficient for VS neuronal identity and migration, but this is accomplished in postmitotic cells, which require the continued presence of SOX1. Our data also suggest that other SOXB1 members showing expression in specific neuronal populations are likely to play continuous roles from the establishment of precursors to their final differentiation

Altered Nrf2/Keap1-Bach1 equilibrium in pulmonary emphysema

BACKGROUND: Oxidative stress, resulting from the increased oxidative burden and decreased level of antioxidant proteins, plays a role in the pathophysiology of smoking-related pulmonary emphysema. Expression of several antioxidant proteins, such as heme oxygenase-1 (HO-1), glutathione peroxidase 2 (GPX2) and NAD(P)H:quinone oxidoreductase 1 (NQO1), results from an equilibrium created by positive or negative regulation by the transcription factors Nrf2, Keap1 and Bach1, respectively. However, whether the expression of these transcription factors is altered in emphysema and could account for decreased expression of antioxidant proteins is not known. A study was undertaken to investigate the expression and subcellular localisation of Nrf2, Keap1 and Bach1 as potential regulators of HO-1, GPX2 and NQO1 in alveolar macrophages, a key cell in oxidative stress, in lung surgical specimens from non-smokers without emphysema and smokers with and without emphysema. METHODS AND RESULTS: Western blot, immunohistochemical and laser scanning confocal analysis revealed that the Nrf2 protein level decreased significantly in whole lung tissue and alveolar macrophages (cytosol and nucleus) in patients with emphysema compared with those without emphysema. Conversely, Bach1 and Keap1 levels were increased in patients with emphysema. These modifications were associated with a parallel decrease in the expression of HO-1, GPX2 and NQO1 at the cellular level, which was inversely correlated with airway obstruction and distension indexes, and increased macrophage expression of the lipid peroxidation product 4-hydroxy-2-nonenal. Silencing RNA experiments in vitro in THP-1 cells were performed to confirm the cause-effect relation between the loss of Nrf2 and the decrease in HO-1, NQO1 and GPX2 expression. Nrf2/Keap1-Bach1 equilibrium was altered in alveolar macrophages in pulmonary emphysema, which points to a decreased stress response phenotype. CONCLUSIONS: This finding opens a new view of the pathophysiology of emphysema and could provide the basis for new therapeutic approaches based on preservation and/or restoration of such equilibrium